TNFSF15 Antibody - #DF3053

Figure 1 Animal experimental schedule is shown in (A) (n = 6 in each group). Analysis of differentially expressed proteins (DEPs) in OVA-induced asthma (M) compared with control (N). The boxplot shows the distribution of sample expression (B). The pie chart shows the number and proportion of DEPs between groups (C). The volcano plot exhibits the quantitative expression of DEPs between groups (D). The pie chart displays the subcellular localization of DEPs between groups (E). The chart shows the term of the top 20 significance of differential protein enrichment between groups (F). The chart illustrates the biological process, cellular component, and molecular function (G). Top 10 term of difference protein enrichment in the three branches (G). Finally, we combined the differential protein dataset to detect the changes of TNF-a (H) and TL1A/DR3 (I) in the mouse lungs via Western blotting analysis. (J) intensity analysis of (H). (K, L) intensity analysis of (I). Data are expressed as the means ± SD for three independent experiments. #p < 0.05 versus the control group.

Figure 8 Effects of the TL1A/DR3 axis on the EMT in Beas-2B cells were detected. TNF-a (50 ng/mL) stimulation for 48 h as the best cell model based on the above experimental results. The effect of sTL1A on EMT was detected by Western blotting (A, C). The effects of TL1A siRNA on TL1A induced by TNF-a were detected by immunofluorescence (E). Effects of TL1A siRNA on the EMT formation induced by TNF-a were measured by Western blotting analysis (G). (E): magnification 200 ×, scale bar 50 µm. (B, D, F, H) intensity analysis of (A, C, E, G), respectively. Data are expressed as the means ± SD for three independent experiments. #p < 0.05 versus the control group. #*p < 0.05 versus the TNF-a group.

Fig. 2 TL1A levels are increased after TGF-β1 treatment in bronchial epithelial cells. (A) Volcano plots were constructed using fold-change values and adjusted P. The red point in the plot represents overexpressed mRNAs and the blue point indicates down-regulated mRNAs with statistical significance. (B) The expression distribution of TNFSF15, where different colors represent different groups and the vertical axis represents the gene expression distribution. (C and D) Protein expression levels of E-cadherin, N-cadherin, fibronectin, DR3, TL1A, and α-SMA after treatment with different concentrations of TGF-β1 for 48 hours. (E) Immunofluorescence for collagen I, fibronectin, and TL1A after treatment with 20 ng/mL TGF-β1 for 48 hours. (F) The RNA levels of E-cadherin, collagen I, N-cadherin, fibronectin, DR3, TL1A, MMP-9. and α-SMA after treatment with different concentrations of TGF-β1 for 48 hours. (G-H) The levels of secreted TL1A remained unchanged in BEAS-2B cells treated with TGF-β1 at various concentrations and during various time courses. Data are expressed as means ± standard deviation. TGF, transforming growth factor; TL1A, tumor necrosis factor ligand-related molecule 1A; DR3, death receptor 3; MMP-9, matrix metallopeptidase 9; α-SMA, α-smooth muscle actin; GAPDH, glyceraldehyde 3-phosphate dehydrogenase. *P < 0.05, **P < 0.01 versus the control group.

Figure 1 |: TL1A was upregulated in liver tissues and macrophages in mice with hepatic fibrosis. (a) The hepatic fibrosis model was established and verified by H&E and Sirius Red staining (200x). (b) The relative quantification of TL1A mRNA was measured by RT-PCR. (c, d) TL1A expression in the CCl4/WT group was significantly higher than those in the Control/WT and Oil/WT group, which was markedly higher in the CCl4/Tg group than that in the CCl4/WT group detected by Western blot.